Pexophagy: A Model for Selective Autophagy

Germain, Kyla; Kim, Peter K.

doi:10.3390/ijms21020578

Cited by 86 publications

(83 citation statements)

References 188 publications

(245 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Peroxisomes are small single-membrane organelles involved in lipid synthesis and redox homeostasis. Thus, pexophagy is crucial for peroxisome quality control and turnover [ 149 ]. In this process, peroxisome membrane proteins, including the peroxisomal biogenesis factor (PEX) 5 and 70 kDa peroxisomal membrane protein (PMP70), are ubiquitylated by the E3-like ubiquitin ligase complex PEX2-PEX10-PEX12, facilitating recognition by cargo receptors and degradation via autophagy [ 149 ].…”

Section: Selective Autophagy and Its Relevance To Neurodegenerativmentioning

confidence: 99%

Autophagy and Redox Homeostasis in Parkinson’s: A Crucial Balancing Act

Jiménez-Moreno

Lane

2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated primarily from endogenous biochemical reactions in mitochondria, endoplasmic reticulum (ER), and peroxisomes. Typically, ROS/RNS correlate with oxidative damage and cell death; however, free radicals are also crucial for normal cellular functions, including supporting neuronal homeostasis. ROS/RNS levels influence and are influenced by antioxidant systems, including the catabolic autophagy pathways. Autophagy is an intracellular lysosomal degradation process by which invasive, damaged, or redundant cytoplasmic components, including microorganisms and defunct organelles, are removed to maintain cellular homeostasis. This process is particularly important in neurons that are required to cope with prolonged and sustained operational stress. Consequently, autophagy is a primary line of protection against neurodegenerative diseases. Parkinson’s is caused by the loss of midbrain dopaminergic neurons (mDANs), resulting in progressive disruption of the nigrostriatal pathway, leading to motor, behavioural, and cognitive impairments. Mitochondrial dysfunction, with associated increases in oxidative stress, and declining proteostasis control, are key contributors during mDAN demise in Parkinson’s. In this review, we analyse the crosstalk between autophagy and redoxtasis, including the molecular mechanisms involved and the detrimental effect of an imbalance in the pathogenesis of Parkinson’s.

show abstract

Section: Selective Autophagy and Its Relevance To Neurodegenerativmentioning

confidence: 99%

Autophagy and Redox Homeostasis in Parkinson’s: A Crucial Balancing Act

Jiménez-Moreno

Lane

2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…However, in the last years, extensive evidence has reported the key role of autophagy in selective degradation of dysfunctional organelles, protein aggregates, and intracellular pathogens [7,21]. Selective processes including removal of peroxisomes (pexophagy) [22] endoplasmic reticulum (ERphagy) [23], ribosomes (ribophagy) [24], lipid droplets (lipophagy) [25], invading microbes (xenophagy) [26], protein aggregates (aggrephagy) [27,28] and damaged mitochondria (mitophagy) [29] have been reported. As well, selective cargo receptors, such as p62/SQSTM 1, BNIP3L (BCL2-interacting protein 3-like) NBR1 (Next to BRCA1), CALCOCO2 (calcium-binding and coiled-coil domain-containing protein 2), and OPTN (optineurin), needed for selective degradation process, have been widely studied.…”

Section: Main Mechanisms Inducing Autophagymentioning

confidence: 99%

Targeting Autophagy in Breast Cancer

Cocco

Leone

Piezzo

et al. 2020

IJMS

View full text Add to dashboard Cite

Breast cancer is a heterogeneous disease consisting of different biological subtypes, with differences in terms of incidence, response to diverse treatments, risk of disease progression, and sites of metastases. In the last years, several molecular targets have emerged and new drugs, targeting PI3K/Akt/mTOR and cyclinD/CDK/pRb pathways and tumor microenvironment have been integrated into clinical practice. However, it is clear now that breast cancer is able to develop resistance to these drugs and the identification of the underlying molecular mechanisms is paramount to drive further drug development. Autophagy is a highly conserved homeostatic process that can be activated in response to antineoplastic agents as a cytoprotective mechanism. Inhibition of autophagy could enhance tumor cell death by diverse anti-cancer therapies, representing an attractive approach to control mechanisms of drug resistance. In this manuscript, we present a review of autophagy focusing on its interplay with targeted drugs used for breast cancer treatment.

show abstract

“…Thus, autophagy maintains cellular homeostasis by the removal of unfolded proteins and damaged organelles [42][43][44][45]. Autophagy can be executed either non-selectively (macroautophagy or autophagy) or in a selective manner to remove specific organelles, e.g., damaged mitochondria (mitophagy) [46] and peroxisomes (pexophagy) [47]. Autophagy is sustained at a low level in the majority of cells, while its efficiency can be affected by a number of stimuli [48].…”

Section: An Overview Of Autophagy and Autophagy-dependent Cell Deathmentioning

confidence: 99%

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Hartman

2020

IJMS

View full text Add to dashboard Cite

Resisting cell death is a hallmark of cancer. Disturbances in the execution of cell death programs promote carcinogenesis and survival of cancer cells under unfavorable conditions, including exposition to anti-cancer therapies. Specific modalities of regulated cell death (RCD) have been classified based on different criteria, including morphological features, biochemical alterations and immunological consequences. Although melanoma cells are broadly equipped with the anti-apoptotic machinery and recurrent genetic alterations in the components of the RAS/RAF/MEK/ERK signaling markedly contribute to the pro-survival phenotype of melanoma, the roles of autophagy-dependent cell death, necroptosis, ferroptosis, pyroptosis, and parthanatos have recently gained great interest. These signaling cascades are involved in melanoma cell response and resistance to the therapeutics used in the clinic, including inhibitors of BRAF mut and MEK1/2, and immunotherapy. In addition, the relationships between sensitivity to non-apoptotic cell death routes and specific cell phenotypes have been demonstrated, suggesting that plasticity of melanoma cells can be exploited to modulate response of these cells to different cell death stimuli. In this review, the current knowledge on the non-apoptotic cell death signaling pathways in melanoma cell biology and response to anti-cancer drugs has been discussed.

show abstract

Pexophagy: A Model for Selective Autophagy

Cited by 86 publications

References 188 publications

Autophagy and Redox Homeostasis in Parkinson’s: A Crucial Balancing Act

Autophagy and Redox Homeostasis in Parkinson’s: A Crucial Balancing Act

Targeting Autophagy in Breast Cancer

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Contact Info

Product

Resources

About